Reovirus infections are prevalent worldwide in poultry and have been isolated from chickens showing a wide variety of clinical signs including viral arthritis/tenosynovitis, malabsorption syndrome (MAS), pericarditis, myocarditis, and immunosuppression [McNulty et al., “Virus infection of birds,” Reovirus, Chapter 13, pp 181-193 (1993)].
Viral arthritis/tenosynovitis particularly in broiler breeds is the most important disease attributable to reovirus infection. [Nibert et al., Fields Virology 4: p. 1681 (2001)]. It is a persistent viral infection with chronic inflammatory lesions, confined mainly to the hock joints and leg tendons of the chicken. The lesions are localized to synovial structures [Menendez et al., Avian Dis. 19: 112-117 (1975); Ellis et al, Avian Dis. 27: 644-651 (1983); Kibenge et al, Avian Pathol. 14: 87-98 (1985)]; [Nibert et al., Fields Virology 4: p. 1681-1682 (2001)].
Clinical signs/symptoms of reovirus infection have also been associated with malabsorption syndrome (MAS) by several groups [Kouwenhoven et al., Avian Pathol. 7: 183-187 (1978); Page et al., Avian Dis. 26:618-624 (1982); Hieronymus et al., Avian Dis. 27: 255-260 (1983); Goodwin et al, Avian Dis. 37: 451-458 (1993)]. The syndrome is characterized by weight gain depression with non-uniform growth, defective feathering and diarrhea with undigested food and watery content. The pathologic changes mostly include proventriculitis enteritis, pancreatitis and hepatitis. MAS may be caused either by maldigestion or malabsorption or both. Lesions that are found can cause an impairment of digestion by insufficiency of digestive secretions and or an impairment of absorption because of insufficient absorptive capacity. However, there are a variety of pathogenicities of reovirus isolated from MAS as can been seen in the variations of depressed weight gains. [Nibert et al., Fields Virology 4: p. 1681-1682 (2001); Page et al., Avian Dis. 26:618-624 (1982); McNulty et al., Avian Pathol. 13: 429-439 (1984); Decaesstecker et al., Avian Pathol. 15: 769-782 (1986); Kibenge and Dhillon, Avian Dis. 31: 39-42 (1987); Kouwenhoven et al., Avian Pathol. 17: 879-892 (1988); Montgomery et al., Avian Dis. 41: 80-92 (1997) Songserm et al., Avian Dis. 46: 87-94 (2002)]. To date, there has been no disclosure in the prior art of an avian reovirus causing neurological symptoms.
There are several prior art vaccines for known avian reoviruses. Examples of live vaccines include strain S1133 and 2177. Live vaccines in the United States have been developed from various passage levels of avian reovirus strain S1133, isolated and characterized by van der Heide from a field case of tenosynovitis. Strain S1133 was grown serially 235 times in the chorioallantoic membrane (CAM) at 37.degree. C. and then 65 times in chicken embryo fibroblast (CEF) at 32.degree. C. An additional 135 passages were carried out at 37° C. in CEF [van der Heide et al., Avian Dis., 27:698-706 (1983)]. Strain 2177 was isolated and characterized by Rosenberger from a field case of avian reovirus [U.S. Pat. No. 5,525,342]. Strain 2177 was isolated from chickens exhibiting reovirus disease by inoculating tissue samples into embryonated eggs and collecting the yolk fluid. This yolk fluid was then inoculated into CEF and passed 14 times until the cytopathology was observed at which time the virus was plaque purified. This yolk fluid was then propagated in embryonated eggs to produce a stock of virus. The stock was found to be non-pathogenic and was titled strain 2177. To date, no reovirus has been able to be grown/cultured immediately upon Vero cells without adaptation. [Nibert et al., Fields Virology 4: pp. 1681-1682 (2001)]. The most common method is propagation in embryonated chicken eggs. There is disclosure in the prior art of an orthoreovirus from an Australian flying fox, a mammalian reovirus, having some characteristics of an avian orthreovirus (reovirus) that is able to be propagated in mammalian cells. [Nibert et al., Fields Virology 4: p. 1682 (2001)]. However, there is no disclosure in the prior art of an avian reovirus that is able to be propogated in a mammalian cell without adaptation. [Nibert et al., Fields Virology 4: p. 1682 (2001)]. As well, the prior art does not disclose a method of treating and/or preventing neurological symptoms in poultry caused by an avian reovirus. Accordingly, the art field is in search of a method to treat and/or prevent neurological symptoms cause by an avian reovirus.
Recently, van Loon et al [Veterinary Quarterly, 23: 129-133 (2001)] described the isolation and identification of a new class of reoviruses, the so-called enteric reovirus strains (ERS). ERS was isolated from broilers in showing high mortality. Those broilers came from parent flocks that were well vaccinated against reovirus infections. It became clear that ERS was a new serotype of reovirus since the virus could not be neutralized by known reoviruses using the plaque reduction test [van Loon et al., Veterinary Quarterly, 23: 129-133 (2001)]. Furthermore, characterization of ERS with a panel of monoclonal antibodies revealed that these strains showed a distinct panel pattern compared to reovirus strains that have been described in the literature previously [Hieronymus et al., Avian Dis. 27: 246-254 (1983); Johnson, Avian Dis. 16: 1067-1072 (1972); Olson et al., Am J Vet Res. 18: 735-739 (1957); Rosenberger et al, Avian Dis. 33: 535-544 (1989); van der Heide et al., Avian Dis. 18: 289-296 (1974)]. The novel antigenic class of reovirus was further identified by the art-accepted practice of a plaque reduction assay, U.S. patent application No. An explanation of a plaque reduction assay may be found in an article by Nersessian et al. (J. Vet. Res. N50, 1989, pp. 1475-1480). The article confirms the heterogenic immunological character of avian reovirus and validates the use of plaque reduction assays for determining and characterizing antigenic relationships (including, but not limited to, similarities and differences) between reovirus isolates. Upon screening for Reoviruses in the field, it was observed that ERS type strains were also present in The Netherlands, Belgium, Ireland, United Kingdom, Spain, Germany, Italy, USA, Argentina, United Arabic Emirates, South Africa, The Philippines and Indonesia. These ERS type strains were usually isolated from birds with MAS. Studies of the pathogenicity and dissemination of ERS in specific pathogen free (SPF) chickens demonstrated that ERS was able to induce a high mortality, tenosynovitis (unpublished observations) and MAS [van Loon et al., Veterinary Quarterly, 23: 129-133 (2001)]. Also in commercial broilers with maternally derived antibodies against reovirus, van Loon et al [Veterinary Quarterly, 23: 129-133 (2001)] showed a growth retardation of respectively 35% and 25% in broilers inoculated at day old or at 7 days old. Further study and evaluation of this novel class has yielded other surprising characteristics.